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7
EXPOSURE TO ENVIRONMENTAL
TOBACCO Smoke
Involuntary exposure to environmental tobacco smoke (ETS),
or passive smoking, has been extensively investigated with re-
spect to its potential health effects, particularly on respiratory
health. There is a significant body of research on its potential ef-
fects regarding the incidence, prevalence, and exacerbation of es-
tablished asthma. While attention has focused upon possible as-
sociations with childhood asthma, associations with asthma in
adults also have been investigated. The following analysis relies
heavily on several very detailed and comprehensive reviews, in-
cluding those of the U.S. Environmental Protection Agency (EPA)
(U.S. EPA, 1992), the California EPA s Office of Environmental
Health Assessment (California EPA, 1997), the World Health Or-
ganization (WHO) International Consultation on Environmental
Tobacco Smoke (ETS) and Child Health (WHO, 1999), the report
of the United Kingdom s Scientific Committee on Tobacco and
Health (SCOTH, 1998), and the series of ten meta-analyses (to
date) of the health effects of ETS by Cook, Strachan, and col-
leagues (Anderson and Cook, 1997; Cook et al., 1998; Cook and
Strachan, 1997, 1998, 1999; Strachan and Cook, 1997, 1998a-1998c).
263

264
CLEARING THE AIR
DEFINITION OF ENVIRONMENTAL TOBACCO SMOKE (ETS}
Environmental tobacco smoke has been defined (Daisey et al.,
1994) as:
. . . the smoke to which non-smokers are exposed when they are in
an indoor environment with smokers. It is composed largely of
sidestream tobacco smoke (SS), the smoke emitted by the smolder-
ing end of a cigarette between puffs, with minor contributions from
exhaled mainstream smoke (the smoke which is directly inhaled by
the smoker) and any smoke that escapes from the burning part of
the tobacco during puff-drawing by the smoker. ETS differs from
SS in that it is highly diluted and dispersed within a room and it
undergoes aging.
Tobacco smoke contains many chemical products with known
or suspected adverse health effects. These products include eye
and respiratory irritants, systemic toxicants, mutagens and car-
cinogens, and reproductive toxicants (California EPA, 1997~. ETS
consists of solid particulates, and semivolatile and volatile organic
compounds (VOCs). The solid particulates have a mean diameter
of 0.32,um (National Research Council, 1986~. "The aging process
includes volatilization of nicotine, which is present in the particu-
late phase in mainstream smoke but is almost exclusively a com-
ponent of the vapor phase of ETS" (U.S. EPA, 1992~. The mean
and standard deviation of the total emission factor for PM 2 5, de-
termined for six commercial cigarettes and Kentucky reference
cigarette 1R4F, is 8,100 + 2,000 ,ug per cigarette. Bacterial endot-
oxin (lipopolysaccharide), previously associated with environ-
mental lung diseases, has been reported to be a respirable con-
stituent of both mainstream and sidestream smoke (Hasday et al.,
1999~.
Significant amounts of nearly 30 volatile organic compounds
have been measured, including acetaldehyde, formaldehyde,
nicotine, 3-viny~pyridine, toluene, pyridine, benzene, pyrrole, xy-
lene, 2-butanone (methyl ethyl ketone iMEK]), phenol, and oth-
ers. Many of the more volatile VOCs (such as aldehydes) remain
in the air for prolonged periods of time following the smoking of
a cigarette (at least four hours) and do not appear to undergo
significant chemical reactions within this period. Some of the less
volatile compounds and particulates appear to decrease over time

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
265
due to deposition as well as ventilation effects. With the excep-
tion of nicotine, the emission factors for VOCs are significantly
greater in ETS than in SS (U.S. EPA, 1992~.
Additional information on the physical and chemical proper-
ties of ETS and the biological activities can be found in the U.S.
and California EPA reports (California EPA, 1997; U.S. EPA, 1992~.
FACTORS CONTROLLING EXPOSURE TO ETS
Variations in Concentration of ETS in Indoor Environments
Exposure Assessment
Nicotine and particulate matter (PM), in addition to carbon
monoxide, have been the constituents most extensively measured
as a means of assessing ETS concentrations in indoor air. Nicotine
is considered an adequate tracer for PM under certain conditions,
and, possibly, for VOCs ranging from slightly to very volatile
compounds (Dailey, 1999~. Among the documented conditions
influencing the concentration of nicotine are emission rates, ven-
tilation, and (for VOCs/SVOCs) resorption and Resorption from
surfaces (Dailey, 1999~. The EPA (1992) and Guerin et al. (1992)
summarized more than 25 studies of nicotine concentration in
more than 100 different indoor environments and found that the
average concentrations of nicotine ranged from 0.3 to 30,ug/m3, a
hundredfold difference. In residences with one or more smokers,
the typical range was from 2 to 10 ,ug/m3, typically being higher
in winter than in summer. Bars and smoking sections of commer-
cial airplanes recorded the highest levels up to 50-75 ,ug/m3,
although nonsmoking regulations and ordinances have signifi-
cantly altered this. In general, the concentrations of nicotine have
been found to increase with the number of smokers and number
of cigarettes consumed in a given indoor environment (U.S. EPA,
1992~.
One study involving personal monitor measurement of
approximately 100 individuals in 16 metropolitan areas in the
United States reported mean 24-hour time weighted average nico-
tine concentrations of 3.28 ,ug/m3 for those exposed to ETS both

266
CLEARING THE AIR
at work and away from work; 1.41,ug/m3 for those exposed away
from work only; 0.69 ,ug/m3 for those exposed at work only; and
0.05 ,ug/m3 for those exposed at neither location Jenkins et al.,
1996; Jenkins and Counts, 1999~. Particulate concentrations, un-
like nicotine, are not specific to ETS as a source. However, al-
though not unique to the combustion of tobacco, the quantity of
respirable particulates produced by cigarette smoking, is large-
significantly greater than the amounts produced by other com-
mon combustion sources within the home, such as wood-burning
fireplaces, gas stoves, and kerosene space heaters (California EPA,
1997~. Respirable suspended particles in homes with at least one
smoker average about 20-100 ,ug/m3 higher than the levels in
similar nonsmoking homes. The highest concentrations have been
reported in restaurants and bars a maximum of 1,379,ug/m3 and
a range of average concentrations of 35-986 ,ug/m3 (U.S. EPA,
1992~. Ott et al. (1996) documented a 77°/O decrease in the average
concentration of respirable suspended particles in a northern
California tavern after a prohibition against smoking was insti-
tuted. In addition to the influence of the number of smokers and
the amount smoked on the concentration of ETS in a given indoor
environment, concentration is affected by the ventilation rate.
Long-term exposure to ETS has been of most concern from
the standpoint of effects on lung development and cancers. How-
ever, ETS concentration varies over an extreme spatial and tem-
poral range in indoor and outdoor environments, making it in-
feasible to comprehensively assess the ETS exposure history of an
individual over their lifetime by direct exposure assessment or
air sampling in all of the relevant environments. Critical aspects
of this history can, however, be determined and more compre-
hensive and accurate assessment is often feasible for infants and
very young children. Because of the difficulties involved, epide-
miologists have tended to use questionnaires and interviews to
determine individual history with regard to ETS exposure, classi-
fying people into categorical groups to provide a semiquantitative
measure of exposure. Direct measurement of exposure at or near
the breathing zone is often done via personal monitors and can
provide an assessment of integrated exposure, but this is feasible
for monitoring only over a relatively limited period of time.

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
Biomarkers of Exposure
267
The most direct assessment of exposure involves the measure-
ment of ETS constituents or their breakdown products in body
fluids. To date, the most reliable of these biomarkers is cotinine, a
metabolite of nicotine (Benowitz, 1999~. Cotinine has an average
half-life of approximately 16-19 hours (Benowitz and Jacob, 1994;
larvis et al., 1988), making it highly useful for the assessment of
integrated ETS exposure over the two to three days prior to the
measurement. In infants and children, the half-life is appreciably
longer, from approximately 40 hours in children more than 18
months old to approximately 65 hours in neonates (U.S. EPA,
1992~. Because urinary cotinine excretion varies markedly among
individuals as a result of renal function, urinary flow rate, and
urinary pH (Benowitz et al., 1983), results often are expressed as
nanograms of cotinine per milligram of creatinine, rather than
simply in nanograms per milliliter of fluid. However, the produc-
tion of creatinine is a function of muscle mass; hence excretion
varies with age, sex, and other individual factors. In particular,
the low level of creatinine produced in children means that the
cotinine-to-creatinine ratios in children may fall into the range
reported for active smokers (Watts et al., 1990~.
The levels of exposure of nonsmokers to ETS are sufficient
that nicotine and cotinine are detectable in their urine, blood, and
saliva (Benowitz, 1996~. Values are typically in the range of 0.5 to
10-15 ng/mL in the saliva and plasma, respectively, of nonsmok-
ers, with urinary concentrations approximately three times
higher as much as 50 ng/mL or more (Guerin et al., 1992; U.S.
EPA, 1992~. A cutoff of 90 ng/mL has been used to distinguish
active smokers from exposed and unexposed nonsmokers
(Cummings et al., 1990), and studies consistently have been able
to distinguish active smokers from exposed and unexposed non-
smokers Jarvis et al., 1987~. It has been more difficult to distin-
guish exposed from non-exposed non-smokers for a variety of
reasons related to the validity of self-reported smoking status and
ETS exposure, variability in nicotine metabolism, variability in
sampling procedures, and the limits of sensitivity of the assay
methods used (Idle, 1990~. Increasing levels of cotinine have been
generally found to be associated with increasing levels of self

268
CLEARING THE AIR
reported ETS exposure (NRC, 1986; U.S. DHHS, 1986; U.S. EPA,
1992~.
As would be expected from the results of measurement of
ambient concentrations of nicotine, the maximum reported expo-
sure levels have occurred in bars and restaurants and on commer-
cial airline flights approximately 30 ng/mg creatinine (Mattson
et al., 1989~. One study in which adults in an enclosed area were
exposed to sidestream smoke from four cigarettes being smoked
simultaneously and injected into the room continuously by ma-
chine, with ventilation conditions equivalent to those in the aver-
age office environment, found the air concentration of nicotine
rapidly reached a stable level of 280,ug/m3. Average nicotine con-
centration in saliva reached a maximum of 880 ng/mL after 60
minutes of exposure, and cotinine concentrations reached 3.4 ng/
mL in serum and 55 ng/mg creatinine in urine, a little more than
six hours after exposure.
A number of studies have compared biomarkers in active
smokers with those in exposed and nonexposed nonsmokers.
larvis and Russell (1984), for example, found mean urinary
cotinine levels in these three groups of 1,390.0,7.7, and 1.6 ma/
mL, respectively (p < .001 between exposed and nonexposed non-
smokers). Cotinine concentrations of self-reported smokers and
nonsmokers have generally been found to overlap.
In infants and children exposed to ETS, levels of cotinine have
been found to be significantly higher in exposed than in
nonexposed children. Direct exposure assessment has detected
cotinine in the urine on the first day of life in neonates of both
active smokers and ETS-exposed nonsmokers with significantly
higher levels in the latter than in neonates of unexposed non-
smokers Jordanov, 1990~. Henderson et al. (1989) found that air
nicotine concentration in the home was significantly associated
with the average log urinary cotinine level (r = 0.68, p = .006~.
Greenberg et al. (1989) found a median concentration of 121 ng
cotinine/mg creatinine (range 6-2,273 ng cotinine/mg creatinine)
in children with any detectable cotinine. Chilmonczyk et al. (1990)
found median levels of urinary cotinine of 1.6 mg/mL in non-
smoking households, 8.9 mg/mL where someone other than the
mother smoked, 28 mg/mL where only the mother smoked, and
43 mg/mL where both the mother and someone else smoked.

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
Exposure Prevalence
269
In reviewing studies of ETS exposure prevalence, the Califor-
nia EPA (1997) concluded, "Taken as a whole, the various studies
[at least 10 separate investigations including large representative
sample surveys] . . . indicate that within California and the United
States, exposure to ETS was widespread during the time period
of the studies (1979 through 1992~. Analysis of ETS exposure
within California indicated that the workplace, home, and other
indoor locations contributed significantly to the exposure of
adults. For children, the home was the most important single lo-
cation contributing to ETS exposure. In all studies using both self-
reporting and a biological marker (cotinine level) as measures of
exposure, prevalence was higher when determined using the bio-
logical marker." It further cited indirect evidence that "the preva-
lence of ETS exposure in the rest of the U.S. population is higher
than that in California."
It is particularly noteworthy that despite aggressive antismok-
ing education and regulation, and documented reductions in
smoking rates (to 16.7% of the adult population in 1995 [CDHS,
1995~), in 1992 an estimated 9.4% of California women pregnant
within the previous five years had smoked throughout pregnancy,
and an estimated 19.6% of those 17 years of age may be exposed
to ETS in their homes (Pierce et al., 1994~. By inference from stud-
ies of adult smoking, it also would appear that the rates may be
appreciably higher in specific subpopulations.
Influence of Activity Patterns on Exposure
The activity patterns of both children and adults have been
studied in relation to exposure to ETS. For all ages, the home is
the location in which the average person spends the most time
921 minutes per day for adults and 1,078 minutes per day for
children in California. Time within the home is spent primarily in
the bedroom an average of 524 minutes per day for adults and
674 minutes per day for children (Wiley et al., 1991~. The next
greatest amounts of time are spent by children in school or child
care (an average of 109 minutes for all children and 330 minutes
for those attending school), in other people's homes (80 minutes

270
CLEARING THE AIR
average and 251 minutes for those doing this), and in-transit (69
minutes overall and 83 minutes for those traveling). Overall, chil-
dren spend an average of 1,230 min. (20.5 hours) each day in-
doors, 141 minutes outdoors, and 69 minutes in enclosed transit.
Infants and other children ages 2 and under spend the most time
indoors (an average of 21.6 hours), but somewhat less in enclosed
transit (48 minutes). For adults, the times are 1,253 minutes in-
doors, 73 minutes outdoors, and 111 minutes in enclosed trans-
portation, with time in the workplace replacing time spent in
school or child care by children.
For children, the home is clearly the most likely source of ex-
posure to ETS and the place that the child is most likely to sleep.
While smoking is not permitted in schools or day care facilities
and is prohibited in some states in licensed child care in private
homes when children are present, the fact that many children are
in nonlicensed child care arrangements or in states or communi-
ties where smoking prohibitions are not well enforced means that
significant regular exposure may occur in home settings. Expo-
sure during travel in the private automobile is another potential
source of exposure.
For adults, research in California (Lum, 1994a, 1994b) has
shown that exposure in the workplace is the most prevalent loca-
tion for exposure of nonsmokers to ETS, with the home as the
second most prevalent location. To the extent that workplaces
adopt antismoking regulations, this exposure source may dimin-
ish in importance. The private automobile represents another po-
tentially significant location for adult exposure.
It is possible for both adults and children to be exposed to
ETS the majority of the time they are indoors, both during the day
and at night. For the average preschool child, this could be virtu-
ally all of the time, for the school-aged child as many as 15.5 hours
a day, and for adults anywhere from 12 hours (for those working
in a nonsmoking environment) to 24 hours for those working as
well as living in environments in which smoking is permitted.
The only reliable exception would be time spent in school, public
buildings, or public transit where smoking is prohibited. There is
no reason to believe that the activity patterns of persons with
asthma differ significantly from those of nonasthmatics, except
for the possibility of their having lower activity levels that could

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
271
result in more time spent indoors and hence greater exposure to
any ETS present in indoor environments. Further, there are ques-
tions as to whether the sensitization of children to allergens (e.g.,
dust mites, cockroaches) in the home environment may be in-
creased by the presence of ETS, as well as whether increased time
spent in the indoor environment, if this occurs, results in greater
exposure to ETS as well as to indoor allergens.
One study of children between the ages of 2 and 12 in Scot-
land, having at least one parent who smoked, found that salivary
cotinine levels were nondetectable in only four children, all of
whom had only a father who smoked (Irvine et al., 1997~. In the
remaining 493 children, the levels ranged from 0.5 ng/mL (barely
detectable) to 21.2 ng/mL, with a mean of 4.35 ng/mL. The au-
thors cite two studies in which levels of 14.3 ng/mL or higher
have been taken as indicative of active smoking by a child. How-
ever, 13 of the 18 children who scored between 14.3 and 21.2 ng/
mL were younger than 6 years of age and are presumed not to be
active smokers. This study found that the age of the child, cotinine
level and self-reported amount smoked in the home by the index
parent, self-reported frequency of smoking in the same room as
the child, whether the index parent's partner smoked, whether
the child had contact with other smokers, the number of persons
per room in the home, and whether the home had a yard or gar-
den were all significantly and independently related to the child's
cotinine level.
EVIDENCE OF A RELATIONSHIP
BETWEEN ETS AND ASTHMA
Action of ETS on the Lungs
Tobacco smoke, whether mainstream, sidestream, or ETS, is a
lung irritant. From a pathophysiologic point of view, active smok-
ing is associated with significant structural changes in both the
airways and the pulmonary parenchyma (U.S. DHHS, 1984), in-
cluding hypertrophy and hyperplasia of the upper airway mu-
cous glands, leading to an increase in mucous production with
associated increased prevalence of cough and phlegm. Chronic
inflammation of the smaller airways also occurs, leading to bron

272
CLEARING THE AIR
chial obstruction. In addition, airway narrowing may occur con-
sequent to destruction of the alveolar walls, decreased Jung elas-
ticity, and development of centrilobular emphysema (U.S. EPA,
1992~. Smoking also may increase mucosal permeability to aller-
gens, increasing total and specific immunogiobulin E (IgE) levels
(Zetterstrom et al., 1981) and blood eosinophi] counts (Halonen et
al., 1982~.
The adverse health effects and pathophysiologic changes as-
sociated with active smoking have been observed at low-dose ex-
posures, suggesting that ETS might have similar adverse effects,
a suspicion that was heightened by the fact that ETS contains
some volatile substances in greater quantities than are found in
mainstream smoke (U.S. EPA, 1992~. In addition, since large pro-
portions of the population are involuntarily exposed to ETS, in-
cluding more susceptible infants and children, the index of suspi-
cion for adverse effects of ETS is high. Exposures early in life,
when the lung is undergoing significant growth and remodeling,
could plausibly alter Jung development and increase the risk of
various respiratory illnesses, including asthma. It is also plausible
that, in addition to the marked susceptibility of young lungs, there
is variable individual susceptibility in other respects, including
genetic predisposition, lung injury such as bronchopulmonary
dysplasia consequent to premature birth, and greater contact with
a primary caregiver who smokes.
Maternal Active Smoking During Pregnancy
Exposure of the fetus to the products of maternal tobacco
smoking is a form of "environmental" exposure to tobacco smoke,
although not in the same proportions as in airborne ETS and not
to all constituents of ETS (notably, not the particulates). It is plau-
sible that virtually all products of active maternal smoking that
enter the bloodstream of the mother, including products arising
from mainstream and sidestream smoke, cross into the fetus
through the placenta with a diffusion gradient. This has been con-
firmed in the case of carbon monoxide (Longo, 1970) and cotinine.
A biomarker for nicotine exposure, cotinine has been detected in
the amniotic fluid of ETS-exposed women and the urine of their
neonates in significantly higher concentrations than in

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
. .
273
nonexposed nonsmoking women Jordanov, 1990~. Transplacen-
tal passage of the bloodborne products of passive maternal ETS
exposure also would be expected, although at lower levels and
with a different chemical com Position than if the mother were an
active smoker.
Active maternal smoking has been associated with reduced
size of the placental arteries (Asmussen, 1979), a reduction in av-
erage birthweight of 75~00 am. (Abell et al., 1991; Asmussen,
1979; Lodrup Carisen et al., 1997; Miiner et al., 1999; Sherwood et
al., 1999; Wang et al., 1997), and altered lung function measured
shortly after birth (Lodrup Carisen et al., 1997~. Small but statisti-
cally significant deficits in forced expiratory volume in one sec-
ond (FEVER and other spirometric indices (forced vital capacity
[FVC], mid expiratory flow iMEF], and end expiratory flow [EEF])
have been fairly consistently demonstrated in school-aged chil-
dren (data reviewed in Cook and Strachan, 1999) and as early as
three days after birth (Lodrup Carisen et al., 1997), thereby
strongly implicating maternal smoking during pregnancy as the
cause of these deficits. However, in Turkey, where there is heavy
smoking by men and virtually none by women, exposure of chil-
dren also has been associated with significant deficits in lung
function (e.g., Bek et al., 1999~. Experimental studies in animals
have demonstrated that ETS exposure of pregnant rats is associ-
ated with reduced Jung volume, number of saccules and septal
crests, and elastin fibers in fetal lungs (Collins et al., 1985~. More
recently, Sekhon et al. (1999) reported that nicotine alone, when
administered to pregnant rhesus monkeys, altered the expression
of nicotine receptors in the developing fetal lung, leading to lung
hyperplasia with structural alterations and reduced complexity
of the gas-exchange surface.
ETS and Children's Respiratory Health
Recent reviews of an extensive body of cross-sectional, case-
control, and longitudinal epidemiologic research on the effects of
parental smoking on children's respiratory health have come to
very similar, although not identical, conclusions. These reviews
include both systematic, quantitative meta-analyses (Cook and
Strachan, 1999) and narrative reviews (California EPA, 1997; U.S.

274
CLEARING THE AIR
EPA, 1992; SCOTH, 1998; WHO, 1999). In updating their earlier
quantitative meta-analysis to include additional studies con-
ducted between April 1997 and June 1998, Cook and Strachan
(1999) summarize their earlier general conclusions (Cook and
Strachan, 1997, 1998; Cook et al., 1998; Strachan and Cook, 1997,
1998a-1998c) as follows:
Overall, there is a very consistent picture with odds ratios for respi-
ratory illnesses and symptoms and middle ear disease of between
1.2 and 1.6 for either parent smoking, the odds usually being higher
in pre-school than school-aged children and higher for maternal
smoking than for paternal smoking.
Virtually all of the evidence with regard to the effects of
chronic ETS exposure in children comes from epidemiologic re-
search, with very limited investigation of acute exposures. True
experimental investigations of controlled acute exposure in cham-
bers has been limited to adults.
Chronic ETS Exposure and Asthma Incidence, Prevalence,
and Severity in Infants and Children
With respect specifically to the prevalence of asthma and res-
piratory symptoms in school-aged children, both the previously
analyzed and the newer studies reviewed by Cook and Strachan
(1999) supported the conclusion that parental smoking is associ-
ated with "increased prevalence of asthma and respiratory symp-
toms in school children" and that "among children with estab-
lished asthma, parental smoking was associated with more severe
disease." Indicators of disease severity for which such an associa-
tion has been documented include emergency room visits, life-
threatening attacks, and symptoms.
As indicated in Table 7-1, among children ages 5-16, pooled
odds ratios (ORB) for asthma prevalence in studies reported
through April 1997 were 1.21 (95% confidence interval [CI] 1.10-
1.34, 21 studies) for either parent smoking from cross-sectional
studies and 1.37 (1.15-1.64, 14 studies) from case-control studies,
1.36 (1.20-1.55, 11 studies) for maternal smoking only, 1.07 (0.92-
1.24, 9 studies) for paternal smoking only, and 1.50 (1.29-1.73, 8
studies) for both parents smoking. Maternal smoking was associ

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
275
ated with an OR of 1.31 (1.22-1.41, 4 studies) for asthma incidence
under age 6 and with an OR of 1.13 (1.04-22, 4 studies) over age 6.
In younger children (0-2 years of age), the odds ratio for
wheezing illness was 1.55 (95°/O CI 1.16-2.08, 5 studies) for either
parent smoking and 2.08 (1.59-2.71, 7 studies) for mother smok-
ing. These data suggest that parental smoking is more influential
as a cause of "wheezy bronchitis" in infants and toddlers than of
later-onset asthma.
There is, at present, some inconsistency with regard to the
interpretation of studies that have attempted to separate the in-
fluence of maternal smoking during pregnancy from postnatal
maternal smoking. Separation of the effects is difficult since those
who smoke during pregnancy are very likely to continue to do so
after the birth of the child, although some smokers may quit dur-
ing the first trimester and abstain for the remainder of the preg-
nancy, often resuming thereafter. One U.S. study of 705 Chicago
fifth graders (Hu et al., 1997) found that maternal smoking dur-
ing pregnancy was more strongly related to doctor-diagnosed
asthma than was current maternal smoking. Similarly, a Scandi-
navian study of nearly 16,000 children 6-12 years of age (Forsberg
et al., 1997) found that asthma attacks, dry cough, and asthma
treatment in the preceding year were inversely associated with
current smoking in the home but positively associated with smok-
ing in the first two years of life. The inverse relationship with
current smoking suggests that parents (at least in Scandinavia)
may modify their smoking behavior as a result of the child's
asthma.
Several observations may be relevant in understanding the
lower odds ratios for asthma prevalence and incidence in school-
aged children than for wheeze in younger children, especially
where the data come from cross-sectional studies and relate to
current smoking in the home. ETS exposure of older children may
be lessened by virtue of the greater amounts of time spent outside
the home and may not reflect their smoke exposure at a younger
age. Cotinine, a marker for smoke exposure, has been shown to
be lower in school-aged than in younger children, among chil-
dren with comparable levels of smoking in the home (Irvine et al.,
1997~.
As already noted, maternal antenatal smoking has been asso

278
CLEARING THE AIR
ciated with reduced size of the placental vessels and decreased
blood flow to, if not oxygenation of, the fetus, a reduction in
birthweight of infants carried to term, and decreased airflow. In
addition, the risks of prematurity, neonatal respiratory distress
syndrome, and bronchopulmonary dysplasia (BPD) are greater
in children of mothers who smoke during pregnancy. Antenatal
smoke exposure is associated with decreased airflow, which is
considered likely to be related to airway size (Hanrahan and
Halonen, 1998), and it has been suggested that postnatal expo-
sure may induce or augment airway inflammation, both of which
could contribute to the observed greater likelihood of develop-
ment of wheezing and respiratory infections in young children
(Cook and Strachan, 1999; U.S. EPA, 1992~. Arguably, this may
also increase the likelihood of both respiratory infections and sen-
sitization to aeroallergens. All of these factors may, especially in
an infant genetically predisposed to allergen sensitization and
asthma, increase the likelihood that a persistent inflammatory
condition will be established in the airways, thus promoting the
development of asthma and perhaps hastening its manifestation.
However, since asthma clearly occurs in children from nonsmok-
ing homes with little or no ETS exposure, the gradual addition of
such children to the pool of "cases" might tend to weaken the
observed association between asthma and ETS exposure among
older children, whether they are considered cross-sectionally or
as a birth cohort followed longitudinally. A possibly more delayed
development of asthma in some non-ETS-exposed children would
not dilute the observed relationship between ETS exposure and
early wheezing.
Dose-Response Relationship Between
ETS Exposure and Asthma
As summarized in Table 7-1 and noted above, the OR for
asthma prevalence when both parents smoke tends to be higher
than when only the mother smokes, which in turn is higher than
when only the father smokes. The presumed explanation is that,
in general, fathers have less intense contact with the child (and/
or that a nonsmoking mother may exert some influence in pro-
tecting the child against ETS exposure due to the father's smok

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
279
in"). The relative risks associated with these four situations with
respect to tobacco smoke in the home (i.e., both parents smoke,
only the mother smokes, only the father smokes, neither parent
smokes) suggests a dose-response relationship to asthma preva-
lence as well as to wheeze, cough, phlegm, and breathlessness.
This further suggests that a reduction in exposure, short of total
avoidance, confers some benefit. However, the OR for either par-
ent smoking and for paternal smoking is still greater than 1, indi-
cating that this level of exposure is not without risk. Moreover,
once asthma is established, the evidence supports the conclusion
that ETS exposure is associated with more frequent asthma exac-
erbations. Although a threshold may exist, there is no evidence as
to what, if any, level of ETS exposure of a child, especially a child
with asthma, could be said to be "risk free."
ETS Exposure and Asthma Incidence in Adults
There do not appear to be any studies linking chronic adult
ETS exposure to adult onset asthma or any findings of an in-
creased prevalence of asthma in adults exposed to ETS compared
to those not exposed. In fact, if adults with asthma purposely
avoided such exposure, a negative association might be observed.
However, one study has shown an increased likelihood of new
onset of wheezing in young adults, as well as children, attribut-
able to maternal smoking during pregnancy, even after control-
ling for exposure in the home and other risk factors (Strachan et
al., 1996~.
Acute ETS Exposure and Asthma Exacerbations
Assessing the contribution of acute ETS exposure to asthma
exacerbations is difficult since, for a significant proportion of ex-
posed individuals, exposure is likely to be chronic (although vari-
able). The evidence from studies comparing reported recent ETS
exposure and cotinine levels in children seen for acute asthma
versus similar children seen for well-child visits is somewhat
equivocal (Ehrlich et al., 1992; Ogborn et al., 1994~. These studies
suffer from small sample sizes and low power. One large study of
adults correlated asthma symptoms with reported daily ETS ex

280
CLEARING THE AIR
posure and reported an OR of 1.61 (95°/O CI 1.06-2.46) for restricted
activity days in relation to ETS exposure level, with a somewhat
higher ratio (2.05; 95°/O CI = 1.78-2.40) for the level of asthma
symptoms associated with having a smoker in the home, suggest-
ing an effect of chronic as well as acute ETS exposure (Ostro et al.,
1994~.
ETS exposure in a chamber under controlled conditions has
been investigated predominantly in adults with asthma, rather
than in children. These studies, which were reviewed in detail by
the California EPA (1997), have shown slight to moderate tran-
sient effects on lung function in at least a portion of participants
but have not demonstrated a consistent effect. The studies had
significant design limitations, including exclusion of participants
who had recently been ill or had brittle asthma and, in many
cases, the use of exposures of an hour or less in duration. A1-
though participants in some of these studies may have been vul-
nerable to the effects of psychological suggestion because re-
searchers did not disguise the concentration of ETS delivered,
others with effective "blinding" of participants had observed ef-
fects.
CONCLUSIONS REGARDING THE HEALTH IMPACTS OF
ETS WITH RESPECT TO ASTHMA
The evidence cited above permits the following conclusions
with regard to the relationships between ETS exposure and
asthma:
· There is sufficient evidence to conclude that there is a
causal relationship between ETS exposure and exacerbations of
asthma in preschool-aged children.
· There is sufficient evidence to conclude that there is an as-
sociation between ETS exposure and the development of asthma
in younger children. In the limited number of studies that have
been able to separate the effects of maternal active smoking dur-
ing pregnancy from the effects of ETS exposure after birth, evi-
dence suggests that while both exposures are detrimental ma-
ternal smoking during pregnancy has the stronger adverse effect.
· There is limited or suggestive evidence of a relationship

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
281
between chronic ETS exposure and exacerbations of asthma in
older children and adults. Limited or suggestive evidence of an
association between acute ETS exposure and exacerbation also
exists for asthmatics sensitive to this exposure.
· There is inadequate or insufficient evidence to determine
whether or not an association exists between ETS exposure and
the development of asthma in school-age children.
EVIDENCE REGARDING MEANS OF
SOURCE MITIGATION OR PREVENTION
Ventilation and Air Cleaning
At present, source control appears to be the only reliably ef-
fective means of preventing ETS exposure. As discussed in Chap-
ter 10, ventilation and air cleaning measures are available that
have the technical capability of reducing the particulate compo-
nents of ETS in indoor environments. However, these measures
would be unlikely to appreciably reduce exposure of the fetus of
a pregnant woman who smokes. Further, there is currently no
direct evidence as to how much a reduction in the concentration
of ETS particulates in a home, if achieved, would reduce the dem-
onstrated adverse effects of ETS exposure on asthma. Also, there
is no evidence regarding the degree of reduction in ETS particu-
late concentration that actually would be achieved through venti-
lation and air cleaning in the homes of smokers who continue to
smoke indoors, even if these were introduced by an aggressive
educational intervention. Any changes in ventilation that smok-
ers did implement might also vary in effectiveness as a function
of season and weather conditions. Nor is it known how such mea-
sures would affect the actual exposure of the residents, particu-
larly children, and how this might vary as a function of who
smokes and how many smokers are in the home. A more thor-
ough discussion of ventilation and air-cleaning technologies is
contained in Chapter 10.
Gas-phase air cleaning systems are available and potentially
effective for some gas-phase constituents of ETS; however, no
proven, reliable, and cost-effective means of air cleaning currently
exists of removing the broad range of gaseous components of ETS

282
CLEARING THE AIR
from the indoor air. Until the components of ETS that affect
asthma are better characterized, including the role, if any, of spe-
cific VOCs, the importance of developing a means for the removal
of ETS-related VOCs as a means of addressing the asthma prob-
lem will remain unclear.
Source Control
If all ETS exposure were eliminated for fetuses, infants, and
children, and for persons of any age who have already developed
asthma, it is reasonable to assume that the population risk of de-
veloping wheezing with respiratory infections and the risk of
asthma exacerbations would decrease to the levels currently ob-
served among similar persons who are not exposed. This conclu-
sion, however, is inferred primarily from the epidemiologic data
comparing persons from homes with smokers to those living in
homes with no smoker. No demonstration has been reported
showing that exposure can be totally eliminated by an educational
intervention, much less that doing so achieves beneficial asthma
outcomes. However, Eisner et al. (1998) have reported an associa-
tion of asthma severity, health status, and health care initiation
with ETS exposure in 451 nonsmoking adults. They also reported
that cessation of ETS exposure at follow-up was associated with
an improvement in the severity of asthma scores and reduced
health care utilization.
Even in accepting the likelihood that a benefit would result
from truly effective elimination of exposure, questions remain
about the extent to which this can be achieved in practice. Suc-
cessful elimination of exposure is dependent on the extent to
which the initiation of smoking can be prevented, especially in
young women of childbearing age; that women who do smoke
can be induced to cease smoking during and following preg-
nancy; that all persons, particularly parents but also other
caregivers and frequent visitors, can be induced not to smoke at
all or not in the environment of a child with asthma; and that
adults with asthma will actually eliminate their exposure to ETS.
The evidence that these changes can be induced by regulatory or
educational means is reviewed below.

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
Regulatory Strategies
283
Where they exist and are enforced, regulatory strategies pro-
hibiting smoking in public buildings, schools and child care fa-
cilities, on public transit, and in the workplace (e.g., offices, plants,
commercial airplanes, restaurants, bars) have clearly been associ-
ated with decreased population exposure to ETS (California EPA,
1997~. Within private homes, however, regulatory strategies have
been deemed unacceptable, except where licensed child care is
being provided. This leaves source control in the major environ-
ment where ETS exposure occurs the home to be addressed
by indirect regulatory forces (e.g., increased cigarette taxes, con-
trols on cigarette advertising, etc.) and by educational or behav-
ioral change methods.
The overall prevalence of cigarette smoking in the United
States declined substantially from 40°/0 in 1965 to 29% in 1987, but
the decline has leveled off and has not reached the public health
goal of 15% set for the year 2000 (U.S. DHHS, 1991~. In 1995, the
overall prevalence of cigarette smoking was 25% (CDC, 1997~. The
decline has been marginal among those with low education aspi-
rations. Of every five persons who use tobacco, four begin before
age 18 (CDC, 1989~. After several years of substantial decline
among adolescents in four ethnic minority groups, smoking
prevalence increased during the l990s among African-American
and Hispanic youth (CDC, 1998~. These trends and the success of
efforts at smoking prevention and cessation among young women
in particular are especially relevant to the issue of avoiding ante-
natal and postnatal exposure of children to maternal smoking.
Adolescent Smoking Prevention and Cessation
School-based programs to prevent the initiation of smoking
can be successful if they include social reinforcement and other
strategies demonstrated to promote behavioral change (Bruvold,
1993~. Moreover, properly designed school smoking policies (i.e.,
multiple components including a greater emphasis on prevention
and less emphasis on cessation) are associated with lower
amounts of smoking in adolescents (Pentz et al., 1989~. It also has
been shown that certain strategies directed at adolescents can

284
CLEARING THE AIR
have an effect opposite from that intended (McKenna and Will-
iams, 1993~.
Success of Smoking Cessation Efforts Directed at Adults
Public health strategies to prevent initiation of smoking and
encourage cessation have clearly been associated with a decline
in smoking prevalence. However, smoking is an addictive behav-
ior with many personal and social factors that support its con-
tinuation. Many unsuccessful strategies to get smokers to quit
have been attempted, notably those based on simply providing
information and/or those directed at the general population of
smokers who have not evidenced an interest in quitting (e.g.,
Gritz et al., 1992~. Programs directed at smokers who are highly
addicted or who initiated smoking earlier in their lives have been
less successful than those directed at shorter-term, less addicted
smokers (Chen and Millar, 1998; Killen et al., 1988; Senore et al.,
1998; Smith et al., 1999~. As overall smoking cessation rates in the
United States have decreased, those who continue to smoke tend
to be heavier smokers (COMMIT, 1995~. However, the compari-
son of less and more successful programs has enabled a distilla-
tion of the components of the more successful approaches. It has
been clearly demonstrated that well-designed smoking cessation
programs, delivered by trained counselors, can be effective in
achieving smoking cessation in adult men and women, including
ethnic and minority groups (AHCPR, 1996~. Such programs are
associated with greater and more sustained short- and longer-
term quit rates than the rates among persons who quit on their
own, without the benefit of such assistance. Cessation programs
are more successful to the extent that they are more intensive,
take account of the varying motivations and level of addiction of
participants, and are attuned to the individual's readiness to con-
sider and initiate cessation attempts.
With regard to smoking cessation attempts in the clinical set-
ting, strong cessation messages from clinicians, structured in rela-
tion to the readiness and personal needs of the patients and utiliz-
ing nicotine replacement therapy and supplementary educational
and behavioral interventions, have been associated with an in-
crease in both initial and sustained quit rates in controlled trials

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
285
(Law and Tang, 1995; Ockene and Zapka, 1997). The Agency for
Health Care Policy and Research (AHCPR) recently reviewed
more than 3,000 scientific articles that addressed the assessment
and treatment of tobacco dependence, nicotine addiction, and
clinical practice in order to develop guidelines for smoking cessa-
tion for primary care and specialist physicians (AHCPR, 1996;
Fiore et al., 1997~. These guidelines emphasize the importance of
several components: nicotine replacement therapy (NRT), social
support from the clinician, and skills training or problem solving
based on practical advice and techniques to help individuals
adapt to life as a nonsmoker. The inclusion of NRT is associated
with pooled ORs of smoking cessation at six months, compared
with a placebo, of from ~1.6 to ~3.0, depending on the method of
delivery. Odds ratios are lowest for gum, rising to ~2.0 for the
transdermal patch, and 2.92 and 3.05 for nasal spray and inhaled
nicotine (Cepeda-Benito, 1993; Fiore et al., 1994; Law and Tang,
1995; Li Wan Po, 1993; Silagy et al., 1994; Tang et al., 1994;
Viswesvaran and Schmidt, 1992~.
Smoking Cessation Interventions in Pregnant Women
As discussed above, maternal smoking, in particular, has been
associated with adverse respiratory and asthma outcomes. In the
United States in 1994,23.1% of all women and 14.6% of pregnant
women smoked (Kendrick and Merritt, 1996~. Special efforts to
obtain cessation in women, particularly pregnant women and
mothers, appear to be warranted. A meta-analysis of randomized
trials of prenatal smoking cessation interventions that measured
effects between the sixth and ninth months of pregnancy con-
cluded that "prenatal smoking cessation interventions increase
rates of smoking cessation during pregnancy" (Dolan-Mullen et
al., 1994~. Haddow et al. (1991), not included in the review, re-
ported only modest success in getting pregnant women to cease
smoking during pregnancy using a cotinine-assisted intervention.
The relative success of such interventions with women of various
ages, ethnicities, and education has not been analyzed, although
most of the reported studies took place with patients seen in pub-
lic clinic settings, suggesting that the results are not limited to
middle- or upper-income and education groups. There is evidence

286
CLEARING THE AIR
that many women who quit smoking during pregnancy resume
soon after delivery (McBride and Pirie, 1990; Mullen et al., 1997~.
Three studies were reviewed that included low birthweight
and other pregnancy outcome measures in addition to smoking
cessation risk ratios. Reduced risk of low birthweight was found
in studies that achieved higher rates of smoking cessation. Al-
though these studies are suggestive of a potential beneficial effect
on respiratory outcomes, no studies to date appear to have inves-
tigated these outcomes directly. Long-term follow-up is also
needed to determine the effectiveness in sustaining cessation af-
ter delivery.
Reduction of ETS Exposure in Children with Asthma by
Source Control Methods Other Than Smoking Cessation
Efforts to reduce the exposure of children, with or without
asthma, by getting family members who smoke and others to limit
their smoking to outside the home or even to certain well-venti-
lated areas within the home appear to face significant challenges
due to the inherent inconvenience to the smoker and the limita-
tions posed by inclement weather and building characteristics.
Nevertheless, it is useful to consider what is known about the
effectiveness of educational programs in achieving the goal of
protecting children from exposure.
Intervention attempts to reduce passive smoking of infants
and children, with or without asthma, have had mixed success.
Greenberg et al. (1994) reported on an intervention designed to
assist families in reducing infants' ETS exposure. The interven-
tion was based on social learning theory and was delivered dur-
ing four nurse home visits within the first 6 months of life. There
was a tendency for nonparticipants to include higher proportions
of mothers who smoked, as well as black, younger, and less edu-
cated mothers. Intervention effects were considered separately for
families where the mother smoked and families where the mother
did not smoke. Among those randomized, when the mother
smoked the intervention was associated with significantly lower
self-reported exposure of the infant to tobacco smoke from the
mother and from nonmaternal household members. Infants
whose mother did not smoke had low reported exposure from

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
287
the outset of the study, and no intervention effect was observed.
This differential self-reported exposure of infants of maternal
smokers was not, however, accompanied by a significant differ-
ential in the cotinine-to-creatinine ratios of the intervention and
control children. In fact, the proportion with detectable urine
cotinine levels tended to increase over the year of follow-up in
both groups. The incidence of all acute lower respiratory illnesses
(ALRIs) and of severe acute respiratory illnesses did not decrease
in the intervention group, and in fact, there was a small but statis-
tically significant difference in all ALRIs favoring the control
group. There was a significant difference in the frequency of per-
sistent lower-respiratory symptoms in the maternal smoking
subsample, but only where the head of household had a high
school education or less. The authors interpret the results as indi-
cating that mothers took steps to protect the infant from exposure
by removing them from the vicinity of the smoker and that the
infants were nevertheless subsequently exposed to residual nico-
tine but not to other ETS products, "which may be more likely
than nicotine to have acute and chronic toxicity for passive smok-
ers." The authors did not discuss whether parental report could
have been biased in the direction of reduced reporting of expo-
sure, and the unplanned subgroup analysis means that the posi-
tive results with regard to persistent lower-respiratory symptoms
are merely suggestive.
Chilmonczyk et al. (1992) reported an unsuccessful phy-
sician's office-based intervention strategy that used feedback from
the physician to the parent on infant urine cotinine measurements
in an attempt to reduce the infant's exposure to ETS. The 6% re-
duction of urine cotinine levels for the intervention group at fol-
low-up two months later was not statistically significant. This lack
of success was in contrast to the investigator's previous success
in getting women to stop smoking during pregnancy based on
feedback on their own urine cotinine levels (Haddow et al., 1991),
suggesting there may be greater motivation and ability of women
to cease smoking and eliminate exposure of their fetus than to
prevent exposure of infants and older children. An earlier unsuc-
cessfu] attempt to reduce passive smoking in infancy was re-
ported by Woodward et al. (1987~.
Hovell et al. (1994) and Wahigren et al. (1997) have reported

288
CLEARING THE AIR
that among children with asthma, a preventive medicine counsel-
ing intervention was associated with a greater reduction in self-
reported and air monitor-verified ETS exposure than a monitored
or usual care control condition. McIntosh et al. (1994) did not re-
port a significant benefit of a cotinine-assisted, minimal-contact
intervention.
Where positive results and promising interventions have been
reported, there is a need for replication and, if possible, extension
to other populations. Extensions of interventions should be made
to populations including those who tend to be more resistant to
cessation efforts and may be more typical of those whose children
are being exposed to significant levels of ETS and are at risk for
poor asthma outcomes for a variety of reasons. Wilson et al. (1996)
i]
have found that both adults with asthma who smoke and smok-
ing parents of children with asthma are less likely than nonsmok-
ers to attend an asthma education program, making it less likely
that they will modify the child's exposure or experience the other
benefits of such asthma education programs.
None of the studies to date that have investigated educational
nterventions to reduce ETS exposure have extended this to in-
clude asthma outcomes either doctor-diagnosed asthma or
wheezing illness incidence, or the prevalence or exacerbations of
established asthma. Until this is done, it leaves unanswered the
question of whether any ETS exposure reduction that may be
achieved is sufficient to alter these disease outcomes, as well as
whether there is any safe ETS exposure level. This is particularly
important when the intervention aims to reduce infant exposure
by means other than cessation of smoking by all caregivers and
others in the child's environment. For this reason it also is impos-
sible to directly answer questions regarding the cost-effectiveness
of mitigation and prevention strategies.
CONCLUSIONS REGARDING ETS SOURCE CONTROL OR
MITIGATION: FEASIBILITYAND BENEFITS
Conclusions Regarding the Effects of
Complete Avoidance of ETS Exposure
Based on reasoning from the epidemiologic evidence pre

EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE
289
sensed above, the following conclusions can be reached regard-
ing the potential benefits of essentially complete avoidance of ETS
exposure, if this could be achieved:
· There is sufficient evidence to conclude that complete
avoidance of ETS exposure would be associated with a lower like-
lihood of exacerbations of asthma in preschool children with es-
tablished asthma.
· There is limited evidence suggesting that complete avoid-
ance of ETS exposure would be associated with a lower likeli-
hood of exacerbations of asthma in older children and adults.
· There is sufficient evidence to conclude that complete
avoidance of ETS exposure, if this could be achieved, would re-
duce the probability of the development of wheezing with respi-
ratory illness in younger children.
· There is limited or suggestive evidence that complete
avoidance of ETS exposure, if this could be achieved, would re-
duce the likelihood of the persistence of asthma or of new-onset
asthma in children and adults.
Conclusions Regarding Mitigation Through Source Control
· There is sufficient evidence to conclude that increased ven-
tilation and air-cleaning methods are technologically capable of
reducing the concentration of ETS particulates in indoor air.
· There is no evidence as to how readily the necessary venti-
lation and air-cleaning methods or technologies would be
adopted and how effectively they actually would be used to re-
duce ETS concentration.
· There is no evidence of whether interventions designed to
encourage the use of the requisite ventilation and air-cleaning
methods would be associated with a reduction in ETS concentra-
tion, in the exposure of persons with asthma to ETS, or in asthma
prevalence or exacerbations.
· There is inadequate evidence to conclude that interven-
tions intended to establish smoke-free homes where a family
member has asthma and to require smokers to smoke only out-
doors are associated with a reduction in ETS exposure or asthma
exacerbations.

290
CLEARING THE AIR
RES"RCH NEEDS
A better understanding is needed of the mechanisms by
which ETS and its individual constituents may
· impair the normal development of the airways in the fetus,
· promote allergic sensitization,
· promote respiratory infections,
· promote early wheezing illness, and
· (possibly) induce pathophysiologic changes that may pro-
mote the establishment of asthma.
Research is also needed to understand the nature of the inter-
actions, both at the population or epidemiologic level and at the
molecular and cellular levels, between the genetic predispositions
to allergic sensitization and bronchial hyperresponsiveness and
ETS exposure as they relate to the development of asthma. The
respective roles of antenatal and postnatal exposure to ETS in the
pathophysiologic changes associated with asthma and other res-
piratory illnesses are in need of further investigation.
Behavioral research also is needed to better understand the
factors that lead to the initiation of smoking in adolescents, espe-
cially young women, and to the maintenance of smoking in preg-
nant women and mothers. Additionally, there is a need to develop
more effective interventions to achieve sustained pre- and post-
natal smoking cessation in pregnant women and mothers, espe-
cially those whose children are at higher risk of developing
asthma due to their family history, socioeconomic status, and
place of residence. Since ETS exposure of children at greatest risk
for adverse asthma outcomes (especially low-income and minor-
ity children of African-American ancestry) may come from other
caregivers as well as the mother or parents (i.e., other family mem-
bers with whom the mother and child live and from day care pro-
viders), interventions must be developed that will be effective in
reducing the child's exposure from all sources. The effectiveness
of ETS exposure reduction interventions in actually improving
asthma outcomes should be evaluated as well.

Since about 1980, asthma prevalence and asthma-related hospitalizations and deaths have increased substantially, especially among children. Of particular concern is the high mortality rate among African Americans with asthma.

Recent studies have suggested that indoor exposures--to dust mites, cockroaches, mold, pet dander, tobacco smoke, and other biological and chemical pollutants--may influence the disease course of asthma. To ensure an appropriate response, public health and education officials have sought a science-based assessment of asthma and its relationship to indoor air exposures.

Clearing the Air meets this need. This book examines how indoor pollutants contribute to asthma-- its causation, prevalence, triggering, and severity. The committee discusses asthma among the general population and in sensitive subpopulations including children, low-income individuals, and urban residents. Based on the most current findings, the book also evaluates the scientific basis for mitigating the effects of indoor air pollutants implicated in asthma. The committee identifies priorities for public health policy, public education outreach, preventive intervention, and further research.

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